N. meningitidis is a non-motile, Gram-negative human pathogen that colonises the pharynx and causes meningitis (and, occasionally, septicaemia in the absence of meningitis). It causes both endemic and epidemic disease. Following the introduction of the conjugate vaccine against Haemophilus influenzae, N. meningitidis is the major cause of bacterial meningitis in the USA.
Based on the organism's capsular polysaccharide, various serogroups of N. meningitidis have been identified, including A, B, C, H, I, K, L, 29E, W135, X, Y & Z. Serogroup A (MenA) is the pathogen most often implicated in epidemic disease in sub-Saharan Africa. Serogroups B and C (MenB & MenC) are responsible for the vast majority of cases in the United States and in most developed countries. Serogroups W135 and Y are responsible for the rest of the cases in the USA and developed countries. Although the capsular polysaccharide is an effective protective immunogen for some serogroups, this approach is unsuitable for immunising against serogroup B.
For serogroup B, a vaccine has proved elusive. Vaccines based on outer-membrane vesicles have been tested, but protection is typically restricted to the strain that was used to make the vaccine (homologous protection). Research and development on serogroup B vaccines continues [1], with a focus on recombinant and subunit vaccines.
Genome sequences for meningococcal serogroups A [2] and B [3,4] have been reported, and the serogroup B sequence has been studied to identify vaccine antigens [e.g. refs. 5 to 10]. Candidate antigens have been manipulated to improve heterologous expression [refs. 11 to 13].
These antigens have been characterised at the level of primary sequence, and many have also been studied for post-translational processing e.g. NarE [14], NadA [15], App [16], GNA1870 [17], etc. However, it is not known how the proteins behave after administration to patients.